Inflammatory chemical mediators during conventional ventilation and during high frequency oscillatory ventilation.

Imai, Yumiko; Kawano, Tsuyoshi; Miyasaka, Katsuyuki; Takata, Masao; Imai, Takasuke; Okuyama, Kazuo

doi:10.1164/ajrccm.150.6.7952613

Cited by 196 publications

(96 citation statements)

References 4 publications

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“…Recentemente, tem sido demonstrado na literatura que mediadores inflamatórios, como o FNT-alfa e as interleucinas, aumentam durante a ventilação mecânica, principalmente quando se empregam volumes correntes elevados 13,14,[21][22][23][24][25] . Naik et al observaram que o início da ventilação mecânica em ovelhas prematuras desencadeou o aumento dos níveis de mediadores inflamatórios, sugerindo que bastam alguns ciclos de ventilação mecâ-nica no prematuro para causar a lesão pulmonar 15 .…”

Section: Reação Inflamatóriaunclassified

Strategies to minimize lung injury in extremely low birth weight infants

Suguihara¹,

Lessa²

2005

J Pediatr (Rio J)

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Como citar este artigo: Suguihara C, Lessa AC. Como minimizar a lesão pulmonar no prematuro extremo: propostas. J Pediatr (Rio J). 2005;81(1 Supl):S69-S78. AbstractObjective: To review the main causes of new bronchopulmonary dysplasia and the strategies utilized to decrease its incidence in extremely low birth weight infants. Sources of data:For this review a MEDLINE search from 1966 to October 2004, the Cochrane Database, abstracts from the Society for Pediatric Research and recent meetings on the topic were used. Summary of the findings:The survival of extremely low birth weight infants has increased significantly due to improvement in both scientific knowledge and technology. This improvement in survival has therefore resulted in an increased incidence of bronchopulmonary dysplasia. The characteristics of bronchopulmonary dysplasia in extremely low birth weight infants, the so called new bronchopulmonary dysplasia are quite different from the classic bronchopulmonary dysplasia described by Northway. This new bronchopulmonary dysplasia has a multifactorial etiology, which includes volutrauma, atelectrauma, oxygen toxicity and lung inflammation. Therapy such as prenatal corticosteroids, exogenous surfactant, nasal continuous positive airway pressure, new mechanical ventilation modalities and gentle ventilation have been used in attempts to decrease lung injury severity. Conclusions:In order to prevent lung injury in extremely low birth weight infants, it is necessary to minimize several factors that induce bronchopulmonary dysplasia and to utilize less aggressive therapeutic strategies. In addition to the current therapy used to decrease lung injury, knowledge of these causative factors may create new therapies that may be fundamental in improving the clinical outcomes of premature infants.J Pediatr (Rio J). 2005;81(1 Supl):S69-S78: Extremely low birth weight infant, bronchopulmonary dysplasia, mechanical ventilation. ResumoObjetivo: Apresentar uma revisão das principais causas da nova displasia broncopulmonar e as estratégias utilizadas para diminuir sua incidência nos prematuros extremos. Fontes dos dados:Para essa revisão, pesquisas foram feitas na MEDLINE (1996 a outubro de 2004), no Cochrane Database, em resumos da Society for Pediatric Research e recentes conferências sobre o tema. Síntese dos dados:A tecnologia e os novos conhecimentos científicos têm aumentado significantemente a sobrevida de prematuros extremos. Esse aumento da sobrevida resultou em aumento da incidência de displasia broncopulmonar. Atualmente, a displasia broncopulmonar é mais freqüentemente observada em recém-nascidos < 1.200 g. As características da displasia broncopulmonar nesses prematuros extremos, atualmente chamada de nova displasia broncopulmonar, são bastante diferentes da clássica descrita por Northway. A nova displasia broncopulmonar tem etiologia multifatorial, como volutrauma, atelectrauma, toxicidade ao oxigênio e reação inflamatória. Terapias como corticosteróide pré-natal, surfactante exógeno, pressão aérea positiva co...

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Section: Reação Inflamatóriaunclassified

Strategies to minimize lung injury in extremely low birth weight infants

Suguihara¹,

Lessa²

2005

J Pediatr (Rio J)

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“…More recently, experimental studies suggested that mechanical ventilation increases pulmonary levels of inflammatory mediators and induces neutrophil accumulation (14)(15)(16). These studies suggest the hypothesis that ventilator-induced lung injury has an inflammatory component.…”

Section: Introductionmentioning

confidence: 95%

Ventilation with high tidal volume induces inflammatory lung injury

Bueno

Santos

et al. 2002

Braz J Med Biol Res

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Mechanical ventilation with high tidal volumes (V T ) has been shown to induce lung injury. We examined the hypothesis that this procedure induces lung injury with inflammatory features. Anesthetized male Wistar rats were randomized into three groups: group 1 (N = 12): V T = 7 ml/kg, respiratory rate (RR) = 50 breaths/min; group 2 (N = 10): V T = 21 ml/kg, RR = 16 breaths/min; group 3 (N = 11): V T = 42 ml/kg, RR = 8 breaths/min. The animals were ventilated with fraction of inspired oxygen of 1 and positive end-expiratory pressure of 2 cmH 2 O. After 4 h of ventilation, group 3, compared to groups 1 and 2, had lower PaO 2 [280 (range 73-458) vs 517 (range 307-596), and 547 mmHg (range 330-662), respectively, P<0.05], higher wet lung weight [3.62 ± 0.91 vs 1.69 ± 0.48 and 1.44 ± 0.20 g, respectively, P<0.05], and higher wet lung weight/dry lung weight ratio [18.14 (range 11.55-26.31) vs 7.80 (range 4.79-12.18), and 6.34 (range 5.92-7.04), respectively, P<0.05]. Total cell and neutrophil counts were higher in group 3 compared to groups 1 and 2 (P<0.05), as were baseline TNF-α concentrations [134 (range <10-386) vs 16 (range <10-24), and 17 pg/ml (range <10-23), respectively, P<0.05]. Serum TNF-α concentrations reached a higher level in group 3, but without statistical significance. These results suggest that mechanical ventilation with high V T induces lung injury with inflammatory characteristics. This ventilatory strategy can affect the release of TNF-α in the lungs and can reach the systemic circulation, a finding that may have relevance for the development of a systemic inflammatory response.

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“…In the lung, IL-8 has been demonstrated to play a crucial role in the inflammatory processes of diffuse panbronchiolitis (27) and fibrosis and adult respiratory distress syndrome (12). Neutrophil recruitment to the lungs might be a critical step in the pathogenesis of ventilator-induced lung injury (18,33). The likely cellular sources of IL-8 in the lung are the respiratory epithelium and alveolar macrophages (16,42).…”

mentioning

confidence: 99%